My Life in Focus*

Manuscript review

2010-02-26T01:19:34-05:00

이 비디오가 과장이 조금 있긴하지만, 그래도 거의 흡사하다.
세상은 조금만 떨어져서 보면 너무 우습다. 눈물이 난다.
보면서 내가 호통하며 웃지만, 그래도 저 고통스러운 과정을 겪어보지 않은 사람은 알 수 없다..흑흑~~

'내가 웃는게, 웃는게 아니야~~~'

히틀러는 행동부터 말투까지 누구와 너무 비슷해서 더 눈물이 난다.

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폭설

2010-02-11T20:25:31-05:00

Boston은 눈이 원래 많이 오는 동네인데,
올해는 이상하게 따뜻하고,
눈도 잘 안온다.
오히려 남부 지방이 폭설로 고생이고, 여기는 정말 맑음이다.
내가 Boston에 맑은 구름을 몰고 왔나...으흐흐흐흐~~~
사실 많은 눈을 예상했는데, 안오니 조금 아쉽다.
이말 했으니까 며칠후에 이말을 한 것이 후회되게끔 하늘에 구멍이 난 것처럼
폭설이 내리겠지...

나의 부정적인 생각.......

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[Orchestra] NEC Philharmonia + Palma

2010-02-05T19:31:33-05:00

New England Conservatory

Donald Palma, who as the coach of NEC's unconducted Chamber Orchestra is ordinarily not visible onstage, steps to the podium tonight as guest conductor with the NEC Philharmonia.

Date: February 3, 2010 - 8:00:PM

Price: Free

Location: NEC’s Jordan Hall

Overture to La forza del destino.
Haydn Symphony No. 98 in B-flat Major,
Mussorgsky/Ravel Pictures at an Exhibition

=========================================================================
Boston이 물가가 비싸기는 하지만,
열심히 알아보면 이런 공짜 공연과 전시회가 많다.
Celebrity의 공연이거나 Boston Sympony는 아니지만,
저 악단 중 열심히 연주하는 학생이나 공연자 한명이
나와 같은 사람들의 작은 응원으로 미래의 Celebrity가 될 수도......
평일 저녁을 먹고 2시간 공연으로 바쁜 하루를 마무리하니
웬지 많은 것을 한 것 같네.

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Boston-Copley Place

2010-01-05T01:15:29-05:00

우리동네라고 부르기는 아직 어색한 Boston

New Year Eve의 Copley Place
오빠가 Copley place는 코를 푸는 곳이라면서
추운 겨울을 더욱 얼려주었다.

오랫만에 어두운데도 불구하고, 사진이 잘 찍혔다.
Boston은 직접보는 것보다 사진빨이 훨씬 좋은 것 같다.

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무제

2010-01-05T01:00:31-05:00

1월 4일 월요일

#1 새해 연휴를 마치고 학교에 돌아가니 몇주 연휴를 마치고 온 동료들이 또 새롭게 보이고,
12월말부터 한산했던 복도는 다시 북적북적해졌다. 새해를 맞으면 더욱 더 활기쳐야하는데, 해가 거듭할 수록
장거리 달리기를 달리고 나서 드는 기분처럼 헐떡거리고 늘어진 기분이든다.
가방 끈이 길어서 그런가? 3월이랑 8월에 활기를 더 되찾는 거 같다. 아니면 점점 곰이 되는 건가? 동면?

#2 나, 운동하는 것 너무 싫어하는데, 속속 자고 있는 근육을 깨우는 운동은 너무 싫은데,
운동을 지속적으로 하면 쉽게 되찾을 수 있는 생활의 에너지라는 결과물은 포기하기 힘들다.
운동을 하면 아침부터가 다른 것 같다. 눈이 뜨자마자 벌떡 일어나지고, 몇시간만 자도 피로가 풀리고,
게을러지는 기분도 안들고 게을러지기도 싫고, 피부는 탄력이 붙고...이 수많은 benefit
그런데 처음에서 말했듯, 속속 자고 있던 근육을 깨우는 그 미묘한 저항적 기분이 들어서, 그것을 희생하기가 싫어서
몇달전부터 운동을 하겠다는 결심은 작심삼일은 커녕 시작도 안했는데,
드디어 오늘 요가 한번 했다. 찌푸둥했던 몸이 좀 풀렸으려나? 내일은 더 자고 싶다는 생각이 안들건가?
모든지 꾸준히...내일도...쭉~

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린지의 V

2010-01-02T01:27:34-05:00

귀여운 린지
볼때마다 새로운 것을 보여주는 린지
불과 7개월 전인데, 점점 성숙해가는구나.

아무도 가르쳐주지 않았다는데,
V는 어디서 배웠는지...
미스테리야~
애들 앞에서 아무것도 못한다는 말이
애들이 새로운 것을 금방 습득해서는 배워서 인가보다.
사진 찍는 저 순간에 누군가가 V를 하며 표정을 지었겠지.
그 상황과 그 손모양이며 어떻게 짧은 시간에 다 습득했는지...
신기해~

이글은 12월 26일로 옮길 예정

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Harvard Square

2010-01-01T23:37:22-05:00

Harvard Square
Harvard의 대학로
시멘트 sidewalk보다는 정감가는 빨간 벽돌길
낡아보이지만, 유럽풍식 건물들이 늘어선 거리

문학이나 철학을 공부하는 학생이라면
많은 사색에 잠길 것 같은데, 이날 비가 와서 더 그렇게 느껴졌을지도...

길을 건너 교문을 들어서면 Harvard Yard.
Harvard University에 제일 오래된 교정

John Harvard가 Harvard의 설립자라고 되어있기는 한데, wiki에 찾아보니 설립자라기보다는 공헌자라고 하네.
Harvard의 신발을 만지면 대대로 Harvard을 간다고 해서,
관광객들이 신발을 하도 문질러서
금빛으로 윤이나네.
그런데 Harvard 학생들은 거기다가 오줌을 싼다고 하네..ㅋㅋㅋ
믿거나 말거나!~

오래된 학교라서 그런지 명문이라 그런지,
건물하나하나가 운치있어보이네.
도서관은 정말 웅장해서 엄숙한 분위기가 났었다.
한번 들어가서 공부(?) 해봐야지.ㅎㅎ

비가 와서 사람이 없고 참 한산했었는데,
나중에 한번 다시 왔는데,
사람들이 너무 많아서 사진찍기가 분주했다.
관광지이기는 한가보다.

이글은 나중에 12월 5일로 옮길 예정

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New York Art Museum

2010-01-01T22:08:40-05:00

혼자 시간 남았을 때
New York가서 Art Museum 순회하였음.
혼자 천천히 구경하니, 봤던 작품도 다르게 보네.
그런데 안타깝게 바보같이 카메라를 안들고 가서
나의 Cell phone카메라로 열심히 찍었음.

언젠가 취미로 그림 그리고 싶다.

이글은 얼마후에 9월 20일로 옮겨질 예정임.

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[기사:New York Times] Old Ideas Spur New Approaches in Cancer Fight

2010-01-01T01:03:38-05:00

Forty Years' War

Old Ideas Spur New Approaches in Cancer Fight

Top of Form

By GINA KOLATA

Published: December 28, 2009

Mina Bissell will never forget the reception she got from a prominent scientist visiting Lawrence Berkeley National Laboratory, where she worked. She gave him a paper she had just published on the genesis of cancer.

“He took the paper and held it over the wastebasket and said, ‘What do you want me to do with it?’ Then he dropped it in.”

That was 20 years ago, and ever since, Dr. Bissell and a few others have struggled for acceptance of what seemed a radical idea: Gene mutations are part of the process of cancer, but mutations alone are not enough. Cancer involves an interaction between rogue cells and surrounding tissue.

The idea seemed messy and unduly complicated. And cancer genes seemed comparatively clear-cut. So it was often ignored or dismissed as researchers focused on genes and on isolated cancer cells growing in Petri dishes in laboratories.

Now, though, more and more researchers are plunging into those murky depths, studying tumors in their cellular environments. And, once they do, they say, they can explain many anomalies of cancer. The new focus on a cancer’s surroundings, researchers say, is a major shift in thinking about why cancer occurs and how to stop it.

As yet, the research has not led to cures, and scientists expect the real fruits of their efforts — if they occur at all — will be years in the future.

But as the war on cancer drags on, nearly 40 years after it began, scientists say new directions are urgently needed. The death rate has barely budged for most cancers, and the gene mutation strategy has so far had a limited effect. That is probably because cancer cells have so many genetic abnormalities. If one mutated gene is attacked, others take over.

So some researchers are taking a fresh look at ideas that were dismissed as folklore — a blow to the breast might spur cancer, an infection might fuel cancer cells, a weak immune system might let cancer spread. They also say the new approach may help explain mysteries, like why the breast cancer rate plummeted when women stopped taking menopausal hormones. One answer may be that hormone therapy changes normal cells of the breast and may allow some tiny tumors to escape from the milk ducts where breast cancer starts.

The basic idea — still in the experimental stages — is that cancer cells cannot turn into a lethal tumor without the cooperation of other cells nearby. That may be why autopsies repeatedly find that most people who die of causes other than cancer have at least some tiny tumors in their bodies that had gone unnoticed. According to current thinking, the tumors were kept in check, causing no harm.

It also may mean that cancers grow in part because normal cells surrounding them allowed them to escape. It also means that there might be a new way to think about treatment: cancer might be kept under control by preventing healthy cells around it from crumbling.

“Think of it as this kid in a bad neighborhood,” said Dr. Susan Love, a breast cancer surgeon and president of the Dr. Susan Love Research Foundation. “You can take the kid out of the neighborhood and put him in a different environment and he will behave totally differently.”

“It’s exciting,” Dr. Love added. “What it means, if all this environmental stuff is right, is that we should be able to reverse cancer without having to kill cells. This could open up a whole new way of thinking about cancer that would be much less assaultive.”

Some companies are taking note. Genentech, for example, is investigating the way some skin, ovarian, colon and brain cancers signal surrounding cells to promote cancer growth. The company has an experimental drug that it hopes might block this signaling.

Others are studying drugs like statins or anti-inflammatory drugs that may act by affecting signals between surrounding cells and cancers. But, says Dr. Robert Weinberg, a cancer researcher at M.I.T., “this is not a clearly articulated scientific agenda, in large part because we still know too little about these signals and how their release is controlled.”

The researchers are cautious. They, more than anyone else, know the blind alleys of cancer research over the past few decades. And no one is suggesting that controlling a tumor’s environment will, by itself, cure cancer.

And they are not discounting cancer-causing genes. But even some who have made their careers studying cancer genes say a tumor’s environment can no longer be ignored.

“I am an unabashed cancer geneticist,” said Dr. Bert Vogelstein, director of the Ludwig Center for Cancer Genetics and Therapeutics at Johns Hopkins. “The genetic alterations in the cancer cells are the proximate cause of the malignancy.”

But, Dr. Vogelstein said, “one cannot fully understand that disease unless one understands” the tumor’s environment.

It can be a reciprocal interaction, especially as cancers grow and become more advanced. The surrounding cells might let cancers start, but once they do, cancers appear to change the surrounding cells to help fuel the cancers’ growth.

“This notion is not a flash in the pan that will come and go,” said Dr. Weinberg, who, in 1981, discovered the first human oncogene, a naturally occurring gene that, when mutated, can cause cancer.

And Dr. Bissell is now hailed as a hero, with an award named after her.

“You have created a paradigm shift,” the Federation of American Societies for Experimental Biology wrote in a letter announcing that she had won its 2008 Excellence in Science award.

Struggle for Acceptance

Dr. Barnett Kramer, associate director for disease prevention at the National Institutes of Health, recently discovered a paper that startled him. It was published in the medical journal The Lancet in 1962, about a decade before the war on cancer was announced by President Richard M. Nixon. In it, Dr. D. W. Smithers, then at Royal Marsden Hospital in London, argued that cancer was not a disease caused by a rogue cell that divides and multiplies until it destroys its host. Instead, he said, cancer may be a disorder of cellular organization.

“Cancer is no more a disease of cells than a traffic jam is a disease of cars,” Dr. Smithers wrote. “A lifetime of study of the internal-combustion engine would not help anyone understand our traffic problems.”

Dr. Kramer said: “I only wish I had read this paper early in my career. Here we are, 46 years later, still struggling with issues this author predicted we’d be struggling with.”

Others say the time was just not right for such ideas. They know, they say, because they were excoriated when they advanced them.

Dr. Bissell said she had struggled for decades to find acceptance for her ideas.

She was not alone. In 1975, not long after Dr. Bissell started her work, another scientist published a hard-to-refute seminal experiment that seemed to indicate that cancer cells could become normal in the right environment.

The scientist, Beatrice Mintz of the Fox Chase Cancer Center in Philadelphia, inserted mouse cancer cells into early mouse embryos. The embryos grew into mice with cells from the cancer, a teratocarcinoma, and cells from the original embryo. The cancer cells had certainly been incorporated into the mouse embryo, but they were defanged, developing normally. Yet the same cancer cells will spread and kill an adult mouse if they are injected under the skin or into the abdomen.

“It was a sensational experiment,” Dr. Mintz said.

Dr. Bissell also thought the experiment was sensational. But she wanted to know why cells would become deadly tumors in one location and not another.

At the time, she was working with Rous sarcoma virus, or R.S.V., which causes fatal tumors in chickens when inserted into cells. Then, one of her postdoctoral fellows, Dr. David Dolberg, unearthed papers suggesting that the cancer virus would behave differently in chicken embryos.

They injected the virus into embryos. The old papers were correct.

“That meant that if you put the virus in cells in an embryo, you don’t get cancer,” Dr. Bissell said. “And if you put it in a chicken, you do.”

Dr. Bissell and Dr. Dolberg’s paper — the one the visiting scientist dropped into a wastebasket, thinking it ridiculous and clearly wrong — was published in the journal Nature in 1984. The scientist was not the only one who scoffed, Dr. Bissell said.

She interprets the response to the sociology of science.

“The people who are successful become vested in their ideas,” Dr. Bissell said. “It becomes extraordinarily difficult for new ideas to find their way.”

But, to her, the R.S.V. experiments were a clarion call.

Sleeping Cells Awakened

Next, Dr. Bissell did an experiment that gave some credence to an old idea oft dismissed.

Over and over, doctors and patients tell stories of injuries that seemed to spur a cancer. A blow to the breast, an operation, and suddenly cancer takes off. It may mean nothing, just an effort to explain the seemingly inexplicable.

Yet some stories end up in publications. For example, says Dr. Michael Baum, emeritus professor of surgery at University College London, there is a report of eight men with advanced testicular cancer who had surgery to remove the tumors, followed by “a sudden and dramatic exacerbation of the disease.” Animal studies find similar effects, Dr. Baum says.

And in breast cancer, he says, observations of women whose cancer accelerated after breast surgery as well as mathematical modeling indicates that surgery at the site of a dormant tumor can spur it to grow. In some unusual cases, chronic inflammation, as can happen with hepatitis B and C viruses, for example, is thought to lead to cancer. The current hypothesis is that chronic liver inflammation can disrupt the normal architecture of cells, allowing cancers that might have lain dormant to thrive.

Most likely, if wounding or inflammation has an effect, it happens only under unusual conditions and if tiny cancers are already present at the site of the wound.

That is what happened when Dr. Bissell did an experiment in chickens.

She knew that when she injected a chicken with R.S.V., the cancer-causing virus, the bird would develop a huge tumor at the site of the injection. But Dr. Bissell had injected the virus into the bird’s blood. Why weren’t there tumors everywhere?

She reasoned it through.

“What do we do when we inject?” Dr. Bissell asked. “Well, we make a wound. We injected the virus in one wing and got a huge tumor. What would happen if we injected the virus in one wing and wounded the other wing?”

She tried it. A huge tumor grew where she had injected the virus and another grew on the other wing where she had made the wound.

Researchers are not saying that infections or simple cuts or most cancer operations will cause cancer or make an existing cancer spread. Most likely, if there is an effect, it happens only if tiny cancers are already present at the site of the injury.

“Obviously it’s more than just surgery,” Dr. Love said. “The majority of people who have surgery don’t have a problem.”

But, she said, the findings tell her that if people have a choice of more or less invasive surgery — laparoscopy versus open surgery, for example — they might want to choose the less invasive.

“And I say this as a surgeon who likes to put her hands in and muck around,” Dr. Love added.

Dr. Kramer said that made sense, but added: “Would I avoid operations? No. I don’t think the evidence is good enough.”

A bigger risk than wounding, Dr. Bissell says, is simply aging, in which cell architecture crumbles, which is why people get wrinkles, for example. And it may be why most cancer occurs in older people.

“I think that this is unfortunately a fundamental problem in cancer,” Dr. Bissell said. “Unfortunately, we haven’t discovered what to do about aging.”

One of the great mysteries about breast cancer is what to make of tiny tumors known as ductal carcinoma in situ, or D.C.I.S. They are so small they cannot be felt and so common they account for about a quarter of tumors found with mammograms. But, studies show, most stay in the milk ducts, where they originate, never spreading to the rest of the breast where they can become lethal.

The problem is that doctors cannot tell the dangerous D.C.I.S. tumors from the harmless ones, so they treat all such tumors as if they were dangerous.

Dr. Kornelia Polyak of Harvard Medical School, like many others, thought she could solve the problem. From the start, she thought, dangerous D.C.I.S. might have genes different from those of D.C.I.S. that remains harmlessly enclosed in milk ducts. Dangerous D.C.I.S. would look like invasive breast cancer cells and harmless D.C.I.S. would not.

But, she found, D.C.I.S. cells looked just like cells from aggressive breast cancers — gene expression patterns, mutations and cell maturation patterns were all the same.

“It’s just that one tumor is inside the duct, and the other is outside the duct,” Dr. Polyak said.

“That was surprising,” she added. “Why is it D.C.I.S. if it looks like invasive cancer?”

She looked at cells surrounding D.C.I.S.

The first thing she noticed was that when D.C.I.S. broke free of a milk duct, the duct’s outer layer had broken down. It could be that the duct falls apart because the cancer is bursting out. Or it could be that the cancer is escaping the duct because the outer layer disintegrated — which is what her research showed. As long as the milk duct is intact, D.C.I.S. cells cannot escape.

She also found that when breast tissue is injured, wound healing can destroy the crucial outer layer of ducts, allowing D.C.I.S. to escape. That is what happens in animals, and it is her hypothesis that it happens in humans.

It made her ask about biopsies. They are unavoidable, as she knows, because she recently had one herself. And they cannot be a huge factor in causing cancer or millions of women would be getting breast cancer at the site of their biopsies — and they are not.

Still, she worries. “Frankly, this has not been studied extensively,” Dr. Polyak said. “People don’t like to bring it up.”

A Nudge Over Time

The dream of many cancer researchers is to find a way to prevent a cancer cell’s environment from allowing it to grow. They could then prevent cancer.

And in one situation, they might have accidentally stumbled upon a possible method.

The discovery began with a surprise in 2003, when breast cancer rates in women 50 and older suddenly fell 15 percent, after the rates for all women had steadily risen since 1945. The pattern held in 2004.

The drop was traced to the release of a large federal study in 2002 that reported that Prempro, a hormone therapy for menopause that was supposed to keep women healthy and protect them from heart disease, actually made heart disease more likely and slightly increased the risk of breast cancer.

Sales plunged after the report was released, as millions of women stopped taking the drug.

But cancer is supposed to take years, even decades, to develop. How, some asked, could cancer rates drop so quickly?

Could it be possible that the hormone treatment somehow changed the environment of naturally occurring cancer cells and let them progress?

Dr. Karla Kerlikowske, professor of medicine, epidemiology and biostatistics at the University of California, San Francisco, now believes that is a possibility. A combination of estrogen and progestin, like that in Prempro, may change the structure and activity of breast tissue, Dr. Kerlikowske finds, making breast tissue denser, a condition that has nothing to do with how breasts look or feel. Breast density is a cellular structure seen on mammograms and has long been associated with higher cancer risk.

Her hypothesis is that hormone therapy can give “that little bit of nudge over a long enough period to promote breast cancer,” Dr. Kerlikowske said.

For some cancers destined to be aggressive, she suggests, it probably makes no difference if a woman takes hormones because the cancer will spread anyway. But she thinks that “for the average person, it becomes very important.”

That, of course, makes it even harder to figure out cancer.

“If it was easy,” Dr. Polyak said, “we would have done it already.”

Nathan Weyland for The New York Times

Dr. Mina Bissell has been lauded for creating “a paradigm shift” in the study of the genesis of cancer.

Gretchen Ertl for The New York Times

Dr. Kornelia Polyak has studied tiny tumors in the breast that may or may not turn dangerous.

This article has been revised to reflect the following correction:

Correction: December 30, 2009
Because of an editing error, an article on Tuesday about new cancer treatments based on older ideas misspelled part of the name of the university that is home to the Ludwig Center for Cancer Genetics and Therapeutics. It is Johns Hopkins University, not John Hopkins.

http://www.nytimes.com/2009/12/29/health/research/29cancer.html

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Boston에서의 한달

2010-01-01T20:46:17-05:00

이제 Boston에서 지낸지 어느덧 한달이상이 흘러갔다.
그리고 새로운 학교 나간지도 한달이 되어가고...

영화 Julie&Julia 보고 먼지가 약간 쌓여가는 내 블로그에 무엇을 해야겠다는 반상적인 생각을 해서
오늘은 내 새로운 그러나 평범했던 생활을 적어야겠다.
Julie는 365 days. 536 recipes를 직접 테스트해서 블로그에 올렸다는데,
난 그 정도는 아니여도 가끔은 블로그에게 말정도는 걸어줘야되지 않겠어?
그리고 여름에 갔던 Alaska와 Arizona의 여행기도 잊지 않았다는거...

본론으로 가서
한달동안 이삿짐 정리하고 이것저것 사느라 돌아다니고,
Thanksgiving과 Christmas 연휴가 겹쳐서 이유없이 연말분위기에 정신없고...
살던 Pennsylvania보다 조금 더 북쪽이라 많이 추울줄 알았는데,
생각보다 훈훈한 날씨가 계속됐다. 서울보다도 많이 따뜻한 것 같네.
몇번 눈은 왔지만...

학교는 새벽 3시에 출근해서 밤 9시에 퇴근한다는 괴소문과는 다르게
전혀 그런 분위기는 아니였고, 내가 계속 몸담고 있던 "이상한 세계"보다 훨씬 정상(?)적인 세계였다.
누구의 말과는 다르게 "Harvard the Hell"이 아니라 그사람의 Hell을 벗어난 것 같아, 무척 다행이라는 생각이.
정말 다행이야.

시골에서 계속 살다가 이제 집 앞에 바로 전철도 있고,
차를 굳이 타지 않아도 걷는 거리에 생활을 해결할 수 있어서 좋고...
대형마트나 체인점의 레스트랑 보다는 아기자기한 local 가게 다딱다딱 붙어있는 것이 웬지 더 친근하다.
옛날에 서울에 있을 때처럼,
학교 셔틀 타러 뛰거나, 떠날 전철 탈려고 뛸때면,
그 기분은 정말 작은 생활 속의 행복이다.

아직 겨울이고, 한달밖에 안 지나서
Boston이 어떤지 잘 모르지만,
다행히도 지금까지의 시작은 너무 좋다.
틈틈이 열심히 다녀야겠다.
웬지 흥미나는 것이 나를 기다릴 것같아 설레네.

사진은 눈이 많이 와서 주말에 빨래나 할려고 했는데,
동전이 없어서, 동전 바꿀려고 돌아다닐때.

여기 눈은 왜 밟을때 왜 더 뽀드득 소리가 날까?

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